Table 2.

Summary of neuroprotective and deleterious effects of reactive or diseased astrocytes highlighted in this review.

ASTROCYTES
Neuroprotective effects	Deleterious effects
Formation of a glial scar isolating physically the injured area. (Dong and Benveniste, 2001) Permissive substrate for axonal regeneration (by expression of NCAM, proteoglycans) (Mckeon, 1995) Release of NGF that induces axonal sprouting (in vitro: Strauss, 1994; Wu, 1998/ in vivo: Chalmers, 1996) Release of anti-inflammatory cytokines, neurotrophins, growth factors (IGF1) (Dong and Benveniste, 2001; Moisse and Strong, 2006) Release of IGF (Garcia-Estrada, 1992)	Impediment of axonal regeneration by glial scar (Dong and Benveniste, 2001) Specific to ALS: Production of toxic molecules (Kreutzber, 1996; Wyss-Coray and Mucke, 2002), and induction of oxidative stress (Klebanoff, 1992; MacMicking, 1997) Release by mutant SOD1 astrocytes of an unknown toxic factor(s) that selectively kills motor neurons (Di Giorgio, 2007; Nagai, 2007; Vargas, 2006) Elevations in both basal and TNF-α stimulated levels of proinflammatory PGE2, leukotriene B4, iNOS and NO, and protein oxidation products in mutant SOD1 astrocytes (Hensley, 2006), upregulated cytokine- and TNF-alpha death-receptor-associated components Induction of motor neuron degeneration by activated astrocyte producing pro-NGF (Domeniconi, 2007), Beta-NGF in cooperation with NO (Pehar, 2004) or NGF oxidized by peroxynitrite (Pehar, 2006) in a p75-NTR – dependent mechanism Increase in the astrocyte production of D- serine, an NMDA receptor co-agonist. (Sasabe, 2007) Indution of PGE2 signaling associated with Cox-1, Cox-2 and iNOS (Liang, 2008) Specific to SMA: Induction of oxidative stress (Araki, 2003)